Publications by authors named "Litao Yi"

3 Publications

  • Page 1 of 1

Berberine administrated with different routes attenuates inhaled LPS-induced acute respiratory distress syndrome through TLR4/NF-κB and JAK2/STAT3 inhibition.

Eur J Pharmacol 2021 Oct 17;908:174349. Epub 2021 Jul 17.

Pharmaceutical Research Center, Xiamen Medicine Research Institute, Xiamen, 361008, Fujian province, PR China.

Accumulating evidence showed that berberine possessed the anti-inflammatory action in various diseases caused by inflammation. However, it was still unclear whether both inhalation and injection with berberine produced pulmonary protective role in acute respiratory distress syndrome (ARDS). This study was aimed to evaluate the effects of both administration routes including inhalation and injection with berberine in ARDS induced by lipopolysaccharide (LPS) inhalation. Histopathological examination and weight of lung were evaluated. Phosphorylation of NF-κB, JAK2 and STAT3 were measured to assess the activity of inflammation related signaling pathways. Proinflammatory cytokines including interleukin (IL)-1β and tumor necrosis factor (TNF)-α in the bronchoalveolar lavage fluid (BALF) and serum were also detected. The results showed that LPS caused the lung injury, while both administration routes with berberine attenuated the injury and improved the pulmonary morphology. In addition, the primary TLR4/NF-κB and secondary JAK2/STAT3 signaling pathways which were activated by LPS in lung were totally inhibited by berberine administration. Moreover, proinflammatory cytokines in both BALF and serum were decreased by berberine. Considering that molecular docking simulation indicated that berberine could bind with TLR4, the present suggested that the inhibition of the inflammation related TLR4/NF-κB and JAK2/STAT3 signaling pathways might be involved in the pulmonary protective effect of berberine in LPS-induced ARDS.
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http://dx.doi.org/10.1016/j.ejphar.2021.174349DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8285933PMC
October 2021

Macranthol attenuates lipopolysaccharide-induced depressive-like behaviors by inhibiting neuroinflammation in prefrontal cortex.

Physiol Behav 2019 05 10;204:33-40. Epub 2019 Feb 10.

Department of Chemical and Pharmaceutical Engineering, Huaqiao University, Xiamen 361021, Fujian Province, PR China; Fujian Provincial Key Laboratory of Biochemical Technology, Huaqiao University, Xiamen 361021, Fujian Province, PR China. Electronic address:

Macranthol is a lignans natural product isolated from Illicium dunnianum Tutch. Our previous studies have shown that BDNF dependent signaling pathway activation was involved in the antidepressant-like effects of macranthol. However, it is not clear whether neuro-inflammation suppression is involved in the effects of macranthol. Therefore, the aim of this present study was to determine whether macranthol affected the neuro-inflammation system in lipopolysaccharide (LPS)-induced mice by measuring pro-inflammatory cytokines and CD11b. Macranthol was orally administrated for successive seven days before a single LPS injection. The behavioral evaluation showed that macranthol prevented LPS-induced depressive-like deficits both in sucrose preference test and forced swimming test. The elevation of serum and prefrontal cortex pro-inflammatory cytokines including interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) was decreased by macranthol pretreatment. In addition, LPS induced the elevation of CD11b in the prefrontal cortex, which was also inhibited by macranthol. Last but not the least, the immunofluorescence found that the number of positive iba-1 cells was also decreased by macranthol. These findings suggest that macranthol could alleviate depressive-like behaviors in mice induced by LPS that are mediated, at least by suppressing microglia-related neuro-inflammation in the prefrontal cortex.
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http://dx.doi.org/10.1016/j.physbeh.2019.02.010DOI Listing
May 2019

Magnolol abrogates chronic mild stress-induced depressive-like behaviors by inhibiting neuroinflammation and oxidative stress in the prefrontal cortex of mice.

Int Immunopharmacol 2018 Jun 5;59:61-67. Epub 2018 Apr 5.

Department of Chemical and Pharmaceutical Engineering, Huaqiao University, Xiamen 361021, Fujian Province, PR China.

Magnolol, the main constituent of Magnolia officinalis, has been shown to produce antidepressant-like effect in rodents. Growing evidence shows that neuroinflammation, oxidative stress and neuroendocrine contribute to the pathogenesis of major depression. Here, the aim of this present study was to determine whether magnolol affected these systems in mice exposed to chronic mild stress (CMS). The ameliorative effect of magnolol on depressive-like symptoms was investigated through behavioral tests, including the classical sucrose preference and forced swimming tests. The behavioral evaluation showed that magnolol reversed the depressive-like deficits both in sucrose preference test and forced swimming test. The elevation of prefrontal cortex pro-inflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) was decreased by magnolol. Consistently, the microglia activation by CMS was also alleviated by magnolol. In addition, the hyperactivity of the hypothalamic-pituitary-adrenal (HPA) axis induced by CMS was attenuated by magnolol. Moreover, the increased lipid peroxidation such as malonaldehyde (MDA) and decreased antioxidant defense enzymes including superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) induced by CMS were also reversed by magnolol. These findings suggest that administration of magnolol could alleviate depressive-like behaviors in CMS mice that are mediated by suppressing neuroinflammation and oxidative stress in the prefrontal cortex.
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http://dx.doi.org/10.1016/j.intimp.2018.03.031DOI Listing
June 2018
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